Greying with age in mice was shown to be due to effects of murine leukemia viruses (MuLV) on melanocyte function. Mice exposed to MuLV by day 8 of gestation developed patterned greying consistent with infection of melanocyte precursors. Mice infected at birth with MuLV developed diffuse greying which could be related to infection of more mature cells in melanocyte differentiation. Induction of neurogenic paralysis by Cas-Br-M MuLV was examined to determine the role of host genes in the development of disease and to determine if immune responses were of importance in resistance to disease induction. Two or more unlinked autosomal dominant loci were shown to control the resistance of some mouse strains to disease. Other results suggest that these genes control the ability of Cas-Br-M to replicate in the central nervous system. Retroviral induction of immunosuppression has gained much attention through the outbreak of AIDS in the United States. A murine retrovirus that induces lymphoproliferation and profound suppression of T cell and B cell responses has been defined as a component in the mixture of viruses recovered from a radiation-induced lymphoma. Activation of the myc oncogene has been implicated in the development of B cell-lineage lymphomas in mouse and man. Mice inoculated with retroviruses containing avian v-myc developed B lineage lymphomas as well as T cell tumors, pancreatic adenocarcinoma, hepatic and pulmonary neoplasms. These results suggest that myc deregulation can affect the growth characteristics of multiple cell lineages.